Abstract
In agreement with previous results, activation of adenosine A 2 receptors was found to inhibit the exocytotic release of elastase and the oxidative burst induced by formyl-MetLeuPhe (fMLP) in human neutrophils. The adenosine analogue 5′- N-ethycarboxamidoadenosine (NECA) was more potent than adenosine (IC 50 14 vs 64 nM). The effects of adenosine and NECA were not influenced by the A 1-adenosine receptor selective antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 300 nM), but were abolished by the non-selective adenosine receptor antagonist 9-chloro-2-(2-furanyl)- 5,6-dihydro-[1,2,4]-triazolo [1,5]quinazolin-5-imine monomethanesulfonate (CGS 15943; 10 μM). Propentofylline per se caused a concentration-dependent inhibition of H 2O 2 production. At 100 μM, propentofylline significantly enhanced the effect of adenosine, but not that of NECA. This effect of propentofylline was shared by the known uptake inhibitor dipyridamole. Neither adenosine nor propentofylline altered fMLP-induced inositol-(1,4,5)-triphosphate (IP 3) formation. The results demonstrate that propentofylline can counteract neutrophil activation, at least partly by enhancing the action of adenosine through blocking its removal, and that the effect is exerted at a step after the initial receptor events.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call